Distinct peritoneal fluid ghrelin and leptin in infertile women with endometriosis and their correlation with interleukin-6 and vascular endothelial growth factor

Rathore, Neha; Kriplani, Alka; Yadav, Raj Kumar; Jaiswal, Urja; Netam, Ritesh

doi:10.3109/09513590.2014.920318

Cited by 21 publications

(16 citation statements)

References 29 publications

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“…Several studies that use similar Methodology in order to observe the VEGF protein produced and not be stuck only gene expression [7,[46][47][48][49] could observe similar results to that obtained in this study.…”

Section: Discussionsupporting

confidence: 94%

p27kip1 overexpression regulates VEGF expression, cell proliferation and apoptosis in cell culture from eutopic endometrium of women with endometriosis

et al. 2014

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We hypothesized that p27(kip1) overexpression can regulate endometriosis cell proliferation, apoptosis and vascular endothelial growth factor (VEGF) expression in the endometrium. The overexpression of p27(kip1) was obtained by transduction of p27(kip1) in primary cultures of endometrium obtained from women with endometriosis tissue with gene therapy technology. First generation bicistronic adenovirus: AdCMVhp27IRESEGFP (Adp27) and AdCMVNull (AdNull) were engineered in order to induce p27(kip1) expression in endometrial cells primary culture. The effect of p27(kip1) overexpression was elucidated through the cell proliferation evaluation and the expression of the cell cycle-related proteins p16, p21, p27, and p53. Cell cycle and apoptosis in endometrial cells from women with and without endometriosis were also evaluated. The VEGF levels were evaluated 1 and 7 days after transduction. The experiments were performed using Immunofluorescence stainings and flow cytometry technique. The cell proliferation statistically diminished markedly following p27(kip1) overexpression in the endometriosis group. This process was accompanied, however, by a statistically significant modulation of the cell cycle-related proteins p16, p21, p27 and p53 markedly increase following p27(kip1) overexpression in the endometriosis group (p < 0.001) and an increase in apoptotic cells was observed. In the endometriosis group, significant downregulation of VEGF expression was observed 7 days after p27(kip1) overexpression, attaining levels strikingly similar to those observed in the control endometrial cells. The findings of this study showed a link between the cell cycle control protein (p27(kip1)) and angiogenesis (VEGF). Our results, also reinforces the background of endometrial dysfunction as part of the origin of endometriosis. We believe that better knowledge of endometrium milieu and the establishment of the link between different, previously describe, altered pathways in this tissue can facilitate future genetic cell therapy.

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Section: Discussionsupporting

confidence: 94%

p27kip1 overexpression regulates VEGF expression, cell proliferation and apoptosis in cell culture from eutopic endometrium of women with endometriosis

et al. 2014

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“…Several studies have already found that the ectopic growth of endometrial-like tissue was depended upon sex steroid hormones 34 and local growth factors 35 such as insulin-like growth factor 1 (IGF-1) 36 or vascular endothelial growth factor (VEGF). 37 Commonly, short cycle length comes along with punctually ovulation and the estrogen level sharply increasing in a short period of time before ovulation. Estrogen has synergistic effects with IGF-1/VEGF and sometimes enhance the effects of IGF-1/VEGF on ectopic endometrial cells proliferation and mitosis, 38 which possibly ended with endometriosis.…”

Section: Discussionmentioning

confidence: 99%

Length of Menstrual Cycle and Risk of Endometriosis

Wei

Cheng

et al. 2016

Medicine

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Endometriosis is a complex disease that affects a large number of women worldwide and may cause pain and infertility.To systematically review published studies evaluating the relationship between menstrual cycle length and risk of endometriosis.We searched the Cochrane Library, PubMed, Web of Science, and EMBASE in databases in July 2014 using the keywords “case–control studies,” “epidemiologic determinants,” “risk factors,” “menstrual cycle,” “menstrual length,” “menstrual character,” and “endometriosis.”We included case–control studies published in English that investigated cases of surgically confirmed endometriosis and examined the relationship between endometriosis risk and menstrual cycle.Eleven articles that met the inclusion criteria included data of 3392 women with endometriosis and 5006 controls. Fixed-effects and random-effects models were used for the evaluation.For the association of risk of endometriosis and menstrual cycle length shorter than or equal to 27 days (SEQ27) or length longer than or equal to 29 days (LEQ29), the odds ratio was 1.22 (95% confidence interval [CI]: 1.05–1.43) and 0.68 (95% CI: 0.48–0.96), respectively.In conclusion, this meta-analysis suggests that menstrual cycle length SEQ27 increase the risk of endometriosis and cycle length LEQ29 decrease the risk.

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“…Human peritoneal fluid (PF) from women with endometriosis show inconsistent protein levels of VEGF, but this may be due to sample size, dilution of PF, or true variability among women. For example, some studies show increased VEGF levels in the PF (Bourlev et al 2010, Xu et al 2013, Szubert et al 2014); however, other studies show no increase in VEGF levels in women with endometriosis compared to healthy women (Barcz et al 2012, Bersinger et al 2012, Rathore et al 2014). Interestingly, more consistency is found in animal models of endometriosis, most likely because of controlled onset of experimental conditions.…”

Section: Pathogenesis and Progression Of Endometriosismentioning

confidence: 99%

Endometriosis: where are we and where are we going?

Greene¹,

Lang²,

Kendziorski³

et al. 2016

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Endometriosis currently affects ∼5.5 million reproductive-aged women in the U.S. with symptoms such as painful periods (dysmenorrhea), chronic pelvic pain, pain with intercourse (dyspareunia), and infertility. It is defined as the presence of endometrial tissue outside the uterine cavity and is found predominately attached to sites within the peritoneal cavity. Diagnosis for endometriosis is solely made through surgery as no consistent biomarkers for disease diagnosis exist. There is no cure for endometriosis and treatments only target symptoms and not the underlying mechanism(s) of disease. The nature of individual predisposing factors or inherent defects in the endometrium, immune system, and/or peritoneal cavity of women with endometriosis remains unclear. The literature over the last 5 years (2010-2015) has advanced our critical knowledge related to hormones, hormone receptors, immune dysregulation, hormonal treatments, and the transformation of endometriosis to ovarian cancer. In this review, we cover the aforementioned topics with the goal of providing the reader an overview and related references for further study to highlight the progress made in endometriosis research, while concluding with critical areas of endometriosis research that are urgently needed.

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Distinct peritoneal fluid ghrelin and leptin in infertile women with endometriosis and their correlation with interleukin-6 and vascular endothelial growth factor

Abstract: The results suggest that ghrelin and leptin might play a key role in pathophysiology of endometriosis, and leptin is associated with inflammation in endometriosis.

Cited by 21 publications

References 29 publications

p27kip1 overexpression regulates VEGF expression, cell proliferation and apoptosis in cell culture from eutopic endometrium of women with endometriosis

p27kip1 overexpression regulates VEGF expression, cell proliferation and apoptosis in cell culture from eutopic endometrium of women with endometriosis

Length of Menstrual Cycle and Risk of Endometriosis

Endometriosis: where are we and where are we going?

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